Prostaglandin E1 attenuates the hypertensive response to tracheal extubation

Abstract

Purpose: Tracheal extubation causes hypertension and tachycardia, which may cause imbalance between myocardial oxygen demand and supply in patients at risk of coronary artery disease. We conducted a randomized, controlled study to evaluate the effects of 0.05 or 0.1 microgram.kg-1.min-1 prostaglandin E1 (PGE1) iv on haemodynamic variables occurring during tracheal extubation and emergence from anaesthesia and compared them in patients receiving either lidocaine or saline.

Methods: Eighty ASA physical status 1 patients undergoing elective surgery were enrolled in the current study. Anaesthesia was maintained with sevoflurane 1.0%-2.5% (ET concentration) and nitrous oxide 60% in oxygen. Muscle relaxation was achieved with vecuronium. The patients were randomly assigned to receive one of four treatments (n = 20 each): saline (control), 0.05 microgram.kg-1.min-1 PGE1, 0.1 microgram.kg-1.min-1 PGE1, or 1 mg.kg-1 lidocaine. PGE1 was infused from completion of surgery until five minutes after tracheal extubation. Changes in heart rate (HR) and blood pressure (BP) were measured during and after tracheal extubation.

Results: In the control group, the HR, systolic BP, and diastolic BP increased during tracheal extubation. Administration of 0.1 microgram.kg-1.min-1 PGE1 and 1 mg.kg-1 lidocaine attenuated the increases in BP although 0.05 microgram.kg-1.min-1 PGE1 failed to do so. The inhibitory effect of the 0.1 microgram.kg-1.min-1 PGE1 on BP was similar to that of lidocaine 1 mg.kg-1 iv. The increase in HR was attenuated by lidocaine but not by PGE1.

Conclusion: The intravenous infusion of 0.1 microgram.kg-1.min-1 PGE1 given during emergence from anaesthesia and tracheal extubation is a useful method for attenuating the hypertension associated with noxious stimuli during this period.